eMedicine Specialties > Radiology > Head/Neck

Optic Neuritis

Pil (Peter) S Kang, MD,, Attending Radiologist, Diagnostic Radiology, Department of Diagnostic Radiology, Walter Reed Army Medical Center; Associate Professor, Department of Radiology, Uniformed Services University of Health Sciences
Fletcher M Munter, MD, Program Director, National Capital Consortium Radiology Residency; Consulting Staff, Department of Radiology, Walter Reed Army Medical Center; Charles Swallow, MD, Department of Radiology, St Marks Hospital

Updated: Jun 23, 2009

Introduction

Background

Optic neuritis is defined as inflammation of the optic nerve. It is one of the causes of acute loss of vision associated with pain. Optic neuritis can be the initial episode for a patient who will subsequently develop multiple sclerosis.

A 43-year-old woman with acute vision loss and eye pain. No prior neurologic symptoms were noted. Axial short tau inversion recovery image demonstrates faint increased signal in the distal left optic nerve.

A 35-year-old woman with acute onset of left eye pain and vision decline. Axial fat-suppressed postcontrast T1-weighted image demonstrates enhancement in the intracanalicular portion of the left optic nerve.

Pathophysiology

The inflammation of the optic nerve is mainly due to demyelination and can be idiopathic and isolated. However, this disease has a very strong association with multiple sclerosis.^5,6 From 15 to 20% of cases of multiple sclerosis manifest as optic neuritis, and 38-50% of patients with multiple sclerosis develop optic neuritis at some point during the course of their disease. According to one of the more well-known long-term, follow-up series of optic neuritis, the risk of development of multiple sclerosis after an episode of isolated optic neuritis was 30% at 5-year follow-up and 38% at 10-year follow-up.

Neuromyelitis optica, also known as Devic disease, is a rare demyelinating process that affects the optic nerve.^7,8,9,10 This disease is frequently misdiagnosed as multiple sclerosis, but it is a separate entity that is distinguished from multiple sclerosis by its severity, by disease location (affects the optic nerves and the spinal cord, sparing the brain), and by cerebrospinal fluid analysis (polymorphonuclear pleocytosis and absence of oligoclonal banding).

Although demyelination is the most common identifiable cause of optic neuritis, other causes of optic nerve inflammation include Lyme disease, tuberculosis, syphilis, and viral agents such as HIV, hepatitis B virus, herpes virus, and cytomegalovirus. Secondary involvement from paranasal sinus infection and orbital cysticercosis has been described. Optic neuritis also may occur as a complication of radiation therapy. Much rarer causes, such as drugs (concurrent etanercept and isoniazid therapy, ethambutol in the setting of end-stage renal disease, interferon alfa), gluten sensitivity, hypereosinophilic syndrome, and vasculitis (giant cell arteritis),¹¹ have been reported in the literature as case reports.

Lesions of the optic nerve in idiopathic and multiple sclerosis–related optic neuritis are similar to the plaques seen in multiple sclerosis of the brain. In acute optic neuritis, lesions are sharply defined areas of myelin sheath loss with relative preservation of the axons. Large numbers of foamy macrophages are present, along with cholesterol ester droplets and abundant lymphocyte and plasma cell accumulations.

In later stages of the disease, the numbers of lymphocytes, plasma cells, and macrophages diminish and astrocytic scar formation occurs. Little remyelination of the damaged axons in lesions is associated with chronic multiple sclerosis, but evidence of oligodendrocyte precursor cells and remyelination attempts in early multiple sclerosis and acute lesions has been documented. This suggests that potential therapeutic interventions that promote myelin formation may play a role in improved recovery.

The lack of remyelination in chronic lesions often is manifested clinically by abnormal visual-evoked potentials, even when Snellen chart visual acuity has returned to normal or near normal in most patients. Functional MRI studies have demonstrated extra-occipital sites of activation during visual stimuli, particularly involving the insula, claustrum, lateral temporal lobe, thalamus, and posterior parietal and orbitofrontal regions. This suggests that a functional reorganization of cerebral responses to abnormal or delayed stimuli from the damaged nerves may occur as an adaptive mechanism. Long-term visual-evoked potential studies suggest that some degree of partial remyelination or ion channel reorganization in the optic nerves may occur up to 2 years after the initial demyelination event. However, this may be counterbalanced by recurrent subclinical episodes of demyelination.

Various genetic and environmental factors are presumed to predispose patients to demyelination as an autoimmune response. The presence of alleles for HLA-Dw2 or HLA-DR2 is a known risk factor in the development of multiple sclerosis and optic neuritis. However, in a Swedish cohort, the allele for HLA-Dw2 was present in only 47% of affected patients. Viral or bacterial infection, stress, and systemic antigens and metabolites have been proposed as possible initiating events that result in autoreactive antibodies and T cells crossing the blood-brain barrier and injuring myelin.¹²

Anatomy

MRI studies have been performed to identify the most common sites of optic nerve involvement in optic neuritis. The nerve can be divided into 5 segments (each with frequency of involvement), including (1) anterior (45%), abutting the optic disc; (2) mid intraorbital (61%); (3) intracanalicular (34%); (4) intracranial prechiasmatic (5%); and (5) chiasmatic segments (2%). Lesions occasionally involve more than one site.

Presentation

The classic triad of optic neuritis consists of (1) loss of vision, (2) eye pain, and (3) dyschromatopsia, which refers to the impairment of accurate color vision. Seventy percent of cases in adults are unilateral. The typical clinical course is that of eye pain and worsening visual function, which progresses over days to weeks. The eye pain usually resolves over days, often as the visual loss begins. The patients usually recover spontaneously, with recovery of visual loss beginning within 2-3 weeks and stabilizing over months.

Additional associated clinical findings may include movement- or sound-induced phosphenes, described as brief flashes of light lasting 1-2 seconds. Reduction in vision may worsen in bright light, a symptom that seems paradoxical. The Uhthoff symptom, described as exercise- or heat-induced vision loss, may occur and has been described in 50% of patients with isolated optic neuritis. Physical examination findings may include an afferent pupillary defect and a swollen optic disc.

Whites of northern European descent are affected 8 times more frequently than blacks and Asians. Whites of Mediterranean ancestry are at intermediate risk. African blacks and Asians are rarely affected. In the United States, the male-to-female ratio for optic neuritis is 1:1.8. The mean age of onset is approximately 30 years, with most patients presenting from age 20-40 years.

The condition is rare in children and is usually related to a postinfectious or parainfectious demyelination.¹³ Optic neuritis in children is less likely to progress to multiple sclerosis, but, in some reports, it has a worse prognosis for full vision recovery. In patients older than age 50 years, optic neuritis is less common and may be mistaken for ischemic optic neuropathy, which is more common in persons in this age group.

Irreversible optic nerve damage occurs in up to 85% of patients; however, this damage often is subclinical. As many as 80% of patients regain at least 20/30 vision, 45% within the first 4 months and 35% within 1 year. Long-term severe vision loss occurs in 20% of patients. This morbidity is separate from that associated with multiple sclerosis.

Occasionally, subclinical optic neuritis is discovered in patients during an evaluation for demyelination suspected for other reasons. These subclinical cases may be detected electrophysiologically by visual-evoked potentials or by careful physical examination if dyschromatopsia, optic disc pallor, and characteristic nerve fiber layer slits are discovered.

The demographics of incidence and prevalence rates of optic neuritis in the United States closely follow those of multiple sclerosis; therefore, the prevalence of optic neuritis is highest among white populations of northern European ancestry, is moderately high in white populations of Mediterranean ancestry, and is low in African black or Asian populations. In the United States, the annual incidence in a predominantly white community is 6.4 cases per 100,000 persons.

Optic neuritis not uncommonly recurs, either in the same or the contralateral eye. The Optic Neuritis Treatment Trial showed that 28% and 35% of patients developed recurrence within 5 and 10 years, respectively. Not surprisingly, recurrence was more common in patients who were subsequently diagnosed with multiple sclerosis. The cumulative probability of developing MS by 15 years after onset of optic neuritis was 50% and was strongly related to the presence of lesions on a baseline non-contrast-enhanced MRI of the brain. Twenty-five percent of patients with no lesions on baseline brain MRI developed MS during follow-up, compared with 72% of patients with 1 or more lesions.^2,14

Most persons with optic neuritis recover spontaneously. Intravenous methylprednisolone therapy has been shown to increase rates of visual recovery but without significant long-term benefit for visual function. Corticosteroids, therefore, are considered for patients who require faster recovery, such as monocular patients, patients with severe bilateral visual loss, or those with occupations requiring high level of visual acuity.

Treatment with corticosteroids and/or immunomodulation agents (eg, interferon beta-1a, interferon beta-1b, glatiramer acetate) can be considered in patients who are at higher risk of developing multiple sclerosis. This is determined predominantly by MRI of the brain.

Preferred Examination

Diffusion-weighted and diffusion-tensor imaging may contribute more data that may prove to have some bearing on treatment and/or on prognosis. The thought is that the loss of anisotropy (manifested by an increase in the apparent diffusion coefficient or decrease in fractional anisotropy) associated with demyelination and/or axonal damage may be more sensitive and/or yield more prognostic information than anatomic imaging findings (size, T2 signal intensity, and enhancement, which suggests loss of the blood-brain barrier due to the underlying pathologic process), which could manifest themselves much later than the findings associated with loss of anisotropy. However, with the current technology, diffusion-weighted and diffusion-tensor imaging of the optic nerves is too time- and labor-intensive for broad clinical application.

The real contribution of imaging in the setting of optic neuritis is made by imaging the brain, not the optic nerves themselves. This is due to the fact that the most valuable predictor for the development of subsequent multiple sclerosis is the presence of white-matter abnormalities. From 27 to 70% (in various studies) of patients with isolated optic neuritis show abnormal MRI findings of the brain, as defined by 2 or more white-matter lesions on T2-weighted images. In the Optic Nerve Treatment Trial, the 5-year risk of developing multiple sclerosis was 16% in patients with normal brain MRI findings, 37% with 1-2 lesions, and 51% with 3 or more lesions. At 10 years, the only statistically significant difference was between no lesions (22% risk) and one or more lesions (56% risk).¹⁴

In addition, information from brain MRI has a potential influence on treatment. It has been shown that in 2-year follow-up of patients with optic neuritis and 2 or more brain lesions on MRIs, patients given intravenous methylprednisolone (as compared with placebo and oral prednisone groups) had a significantly decreased risk of developing multiple sclerosis. Note that this benefit was not maintained at 3 years. In a study using interferon beta-1a (Avonex) in patients with optic neuritis with 2 or more white-matter lesions on MRIs of the brain, a decreased risk of developing multiple sclerosis at 3 years was demonstrated. In those patients who did ultimately develop multiple sclerosis, interferon beta-1a was shown to reduce the disease burden and number of active lesions.

CT scanning has a very limited role in the setting of optic neuritis. Size differences in the optic nerve can be appreciated, but this is neither sensitive nor specific. Contrast-enhanced CT scanning of the orbits may be able to help exclude other orbital pathology, albeit in a limited way relative to MRI, because of the inherently superior soft-tissue contrast resolution yielded with MRI. Certainly, CT scanning of the brain, regardless of whether intravenous contrast material is administered or not, does not yield prognostic and treatment-altering information as does MRI of the brain.

Differential Diagnoses

Brain, Multiple Sclerosis
Orbit, Infection
Sinusitis
Tuberculosis, CNS

Other Problems to Be Considered

Ischemic optic neuropathy
Factitious vision loss
Lyme disease
Compressive optic neuropathy

Magnetic Resonance Imaging

A 43-year-old woman with acute vision loss and eye pain. No prior neurologic symptoms were noted. Axial short tau inversion recovery image demonstrates faint increased signal in the distal left optic nerve.

A 43-year-old woman with acute vision loss and eye pain. No prior neurologic symptoms were noted. Axial fat-suppressed postgadolinium T1-weighted image through the orbit reveals an intensely enhancing segment of the distal left optic nerve (corresponding to the site of subtle increased signal on the image in Image 1 in Multimedia).

A 43-year-old woman with acute vision loss and eye pain. No prior neurologic symptoms were noted. Coronal fat-suppressed postgadolinium T1-weighted image demonstrates intense enhancement within the optic nerve (same patient as Images 1-2 in Multimedia). No significant nerve expansion or enhancement of the adjacent tissues is seen. Note the normal right optic nerve for comparison.

A 35-year-old woman with acute onset of left eye pain and vision decline. Axial fat-suppressed postcontrast T1-weighted image demonstrates enhancement in the intracanalicular portion of the left optic nerve.

A 35-year-old woman with acute onset of left eye pain and vision decline. Axial fluid-attenuation inversion recovery image demonstrates bilateral periventricular white matter lesions. Several additional and similar lesions were seen in other locations (not shown). No history of prior neurologic illness was noted in the patient, but in the setting of acute optic neuritis, the multiple white matter lesions in a number and pattern atypical for patient age were considered supportive of the diagnosis of multiple sclerosis (same patient as Image 4 in Multimedia).

Findings

Bonhomme et al studied the rate of conversion to multiple sclerosis (MS) after a diagnosis of optic neuritis in children (younger than 18 y) who presented with optic neuritis between 1993 and 2004 at the Children's Hospital of Philadelphia. They found that children with brain MRI abnormalities at the time of optic neuritis diagnosis had an increased risk for MS. In the study, they identified 29 children with idiopathic optic neuritis. Eleven of the 29 patients (38%) had white-matter T2/FLAIR lesions in the brain (not including the optic nerves). Eighteen patients were followed for more than 24 months, and 3 of the 18 (17%) developed MS. All 3 patients who developed MS had an abnormal brain MRI scan at their initial presentation of optic neuritis. None of the patients who had normal MRI scans developed MS over an average follow-up of 88.5 months.⁵

Swanton et al investigated patients with optic neuritis to determine the influence of lesion number, location and activity, and non-lesion MRI measures obtained on early scans. At 6-year follow-up, 48% of patients had converted to clinically definite MS, and 52% remained with clinically isolated syndrome. The presence and the number of spinal cord lesions at baseline and new T2 lesions at follow-up were found to be significant independent predictors of higher disability. Disability was also predicted by the presence at baseline of gadolinium-enhancing lesions and the number of infratentorial lesions. Only spinal cord lesions predicted disability in patients converting to clinically definite MS.⁶

Patients in the Optic Neuritis Treatment Trial, who were enrolled between July 1, 1988, and June 30, 1991, were followed up prospectively for 15 years, with the final examination of 389 patients with acute optic neuritis occurring in 2006 to determine development of MS and neurologic disability. The cumulative probability of developing MS by 15 years after onset of optic neuritis was 50% and was strongly related to the presence of lesions on a baseline non-contrast-enhanced MRI of the brain. Twenty-five percent of patients with no lesions on baseline brain MRI developed MS during follow-up, compared with 72% of patients with 1 or more lesions.⁴¹

False Positives/Negatives

Although not specifically relevant to optic neuritis, false-positive results in orbital imaging can result from failure of complete fat saturation related to magnetic susceptibility artifact from dental amalgam and air–soft tissue interfaces, particularly at the inferior margin of the orbit. This is true especially for frequency-selective fat-saturation techniques but less so for inversion recovery sequences.

Fat-saturation failure can mimic orbital edema on multiecho train T2-weighted images or enhancement on fat-suppressed T1-weighted images. Careful evaluation of the tissue surrounding the orbit should reveal the true cause of signal distortion. This artifact should not occur in optic neuritis because the lesion of optic neuritis is confined to the nerve but, potentially, it can mislead the interpreter to conclude that more diffuse orbital inflammation is the cause of vision loss.

Occasionally, the enhancement pattern in optic neuritis may be a peripheral tram-track pattern. Potentially, this can be confused with the enhancement pattern of optic nerve meningioma; however, the optic neuritis pattern should be distinguished from the meningioma pattern by enhancement limited to the nerve, rather than the sheathlike pattern of meningioma, by the absence of significant mass or expansion, and by the clinical features of acute onset vision loss and pain.

Intervention

Medicolegal Pitfalls

• Ophthalmologists often are the first clinicians to evaluate patients with optic neuritis. In the past, many ophthalmology publications suggested that because no specific treatment was available for multiple sclerosis, patients may be worried unduly or damaged by a diagnosis of MRI-supported multiple sclerosis. In light of the newer treatment protocols for patients with early multiple sclerosis, more recent ophthalmology publications assert that the clinician can be held responsible for failure to search for additional evidence of demyelination in the setting of optic neuritis. Radiologists can expect increased interest in imaging optic neuritis for this reason. Occasionally, these are ordered as orbit studies to evaluate optic neuritis. Although already common in many practices, radiologists may wish to consider inclusion of whole-brain imaging as part of a routine orbital imaging protocol.

Multimedia

Media file 1: A 43-year-old woman with acute vision loss and eye pain. No prior neurologic symptoms were noted. Axial short tau inversion recovery image demonstrates faint increased signal in the distal left optic nerve.

Media file 2: A 43-year-old woman with acute vision loss and eye pain. No prior neurologic symptoms were noted. Axial fat-suppressed postgadolinium T1-weighted image through the orbit reveals an intensely enhancing segment of the distal left optic nerve (corresponding to the site of subtle increased signal on the image in Image 1 in Multimedia).

Media file 3: A 43-year-old woman with acute vision loss and eye pain. No prior neurologic symptoms were noted. Coronal fat-suppressed postgadolinium T1-weighted image demonstrates intense enhancement within the optic nerve (same patient as Images 1-2 in Multimedia). No significant nerve expansion or enhancement of the adjacent tissues is seen. Note the normal right optic nerve for comparison.

Media file 4: A 35-year-old woman with acute onset of left eye pain and vision decline. Axial fat-suppressed postcontrast T1-weighted image demonstrates enhancement in the intracanalicular portion of the left optic nerve.

Media file 5: A 35-year-old woman with acute onset of left eye pain and vision decline. Axial fluid-attenuation inversion recovery image demonstrates bilateral periventricular white matter lesions. Several additional and similar lesions were seen in other locations (not shown). No history of prior neurologic illness was noted in the patient, but in the setting of acute optic neuritis, the multiple white matter lesions in a number and pattern atypical for patient age were considered supportive of the diagnosis of multiple sclerosis (same patient as Image 4 in Multimedia).

References

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Keywords

optic neuritis, inflammation of the optic nerve, acute vision loss, multiple sclerosis, human leukocyte antigen Dw2, HLA-Dw2, human leukocyte antigen DR2, HLA-DR2, acute optic neuritis

Contributor Information and Disclosures

Author

Pil (Peter) S Kang, MD,, Attending Radiologist, Diagnostic Radiology, Department of Diagnostic Radiology, Walter Reed Army Medical Center; Associate Professor, Department of Radiology, Uniformed Services University of Health Sciences
Pil (Peter) S Kang, MD, is a member of the following medical societies: Alpha Omega Alpha
Disclosure: Nothing to disclose.

Coauthor(s)

Fletcher M Munter, MD, Program Director, National Capital Consortium Radiology Residency; Consulting Staff, Department of Radiology, Walter Reed Army Medical Center
Fletcher M Munter, MD is a member of the following medical societies: American College of Radiology, American Roentgen Ray Society, American Society of Neuroradiology, Association of Program Directors in Radiology, Association of University Radiologists, and Radiological Society of North America
Disclosure: Nothing to disclose.

Charles Swallow, MD, Department of Radiology, St Marks Hospital
Charles Swallow, MD is a member of the following medical societies: American College of Radiology and American Roentgen Ray Society
Disclosure: Nothing to disclose.

Medical Editor

Barton F Branstetter IV, MD, Associate Professor of Radiology, Otolaryngology, and Biomedical Informatics, University of Pittsburgh; Director of Head and Neck Imaging, Clinical Director of Neuroradiology, Department of Radiology, Division of Neuroradiology, University of Pittsburgh Medical Center
Barton F Branstetter IV, MD is a member of the following medical societies: American College of Radiology, American Medical Association, American Roentgen Ray Society, American Society of Neuroradiology, Pennsylvania Medical Society, and Radiological Society of North America
Disclosure: Nothing to disclose.

Pharmacy Editor

Bernard D Coombs, MB, ChB, PhD, Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District Health Board, New Zealand
Disclosure: Nothing to disclose.

Managing Editor

C Douglas Phillips, MD, Director of Head and Neck Imaging, Division of Neuroradiology, Weill Medical College of Cornell University/New York Presbyterian Hospital
C Douglas Phillips, MD is a member of the following medical societies: American College of Radiology, American Medical Association, American Society of Head and Neck Radiology, American Society of Neuroradiology, Association of University Radiologists, and Radiological Society of North America
Disclosure: Nothing to disclose.

CME Editor

Robert M Krasny, MD, Resolution Imaging Medical Corporation
Robert M Krasny, MD is a member of the following medical societies: American Roentgen Ray Society and Radiological Society of North America
Disclosure: Nothing to disclose.

Chief Editor

James G Smirniotopoulos, MD, Professor of Radiology, Neurology, and Biomedical Informatics, Chairman, Department of Radiology and Radiological Sciences, Uniformed Services University of the Health Sciences
James G Smirniotopoulos, MD is a member of the following medical societies: American College of Radiology, American Roentgen Ray Society, American Society of Head and Neck Radiology, American Society of Neuroradiology, American Society of Pediatric Neuroradiology, Association of University Radiologists, and Radiological Society of North America
Disclosure: Nothing to disclose.

Related eMedicine topics

Optic Neuritis, Childhood

Optic Neuritis, Adult

Multiple Sclerosis (Ophthalmology)

Multiple Sclerosis (Neurology)

Clinical guidelines

Multiple sclerosis. National clinical guideline for diagnosis and management in primary and secondary care.
National Collaborating Centre for Chronic Conditions - National Government Agency [Non-U.S.].  2004.  197 pages.  NGC:003547

EFNS guideline on treatment of multiple sclerosis relapses: report of an EFNS task force on treatment of multiple sclerosis relapses.
European Federation of Neurological Societies - Medical Specialty Society.  2005 Dec.  8 pages.  NGC:005169

EFNS guidelines on the use of neuroimaging in the management of multiple sclerosis.
European Federation of Neurological Societies - Medical Specialty Society.  2006 Apr.  13 pages.  NGC:005479


Clinical trials

Safety and Efficacy Study of Erythropoietin as Add-on Therapy of Methylprednisolone to Treat Acute Optic Neuritis

Atacicept in Optic Neuritis, Phase II

A Randomized, Double-Blind, Placebo-Controlled, Multicenter Study of the Effects of Glatiramer Acetate (GA) on the Retinal Nerve Fiber Layer (RNFL) and Visual Function in Patients With a First Episode of Acute Optic Neuritis (AON). (Octagon)

Biobank For MS And Other Demyelinating Diseases

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